Autor: |
Anggraini Iriani, Andhika Rachman, Rahayuningsih D. Setiabudy, Siti B. Kresno, Aru W. Sudoyo, Mansyur Arief, Alida R. Harahap, Marsya Kaila Fatina |
Jazyk: |
angličtina |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
BMC Molecular and Cell Biology, Vol 24, Iss 1, Pp 1-9 (2023) |
Druh dokumentu: |
article |
ISSN: |
2661-8850 |
DOI: |
10.1186/s12860-023-00495-0 |
Popis: |
Abstract Background Cytopenia is the primary feature of Myelodysplastic Syndrome, even in the presence of hypercellular bone marrow. TNFα is recognized as both a proinflammatory, and proapoptotic cytokine with a well established role in promoting apoptosis in MDS. Therefore, TNFα has the potential to be a valuable biomarker for predicting the progression of cytopenia in MDS. This study aims to establish the role of TNFα exposure in triggering apoptosis through caspase-3 activity in CD34+, CD33+, and CD41 + cells in MDS. Methods This study is an in vitro comparative experimental research. Bone marrow mononuclear cells were isolated as the source of hematopoietic progenitor cells. Subsequently, CD34+, CD33+, and CD41 + cells were exposed to rhTNFα, and the caspase-3 activity was measured using flowcytometry. Results In MDS CD33 + and CD41 + caspase-3 activity of rhTNFα exposed cells was significantly higher than without exposed cells. The opposite result was found in CD34 + cells, where the caspase-3 activity without rhTNFα exposed cells was significantly higher than rhTNFα exposed cells. Conclusion rhTNFα exposure led to an elevation in caspase-3 activity in MDS progenitor cells, especially in those that had differentiated into myeloid cell CD33 + and megakaryocyte cell CD41+, as opposed to the early progenitor cells CD34+. |
Databáze: |
Directory of Open Access Journals |
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